Although the efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) as anti-inflammatory, analgesic and antipyretic agents is well established, there is still an open question as to whether their different pharmacokinetic and pharmacodynamic characteristics do have a different clinical impact in treating rheumatology patients.
The mechanism related to the anti-inflammatory activity of these drugs is mainly related to the inhibition of the cyclo-oxygenase (COX)-2 isoform, whereas inhibition of COX-1 is associated with the side effects of these drugs. However, some NSAIDs exert their anti-inflammatory and analgesic action by additional mechanisms.
The NSAID nimesulide, along with its preferential activity on COX-2 and a short half-life that correlates with a rapid onset of analgesic action, acts also through a variety of COX-independent pathways that contributes to its potent antiinflammatory and analgesic activity.
The pathways affected by nimesulide include inhibition of tumour necrosis factor alpha (TNF-α) release, histamine release, reactive oxygen species production and chondrocyte death. Furthermore, the use of nimesulide has been associated with reduced levels of matrix metalloproteases and other biomarkers of joint destruction, suggesting it may have a protective effect against disease progression.
Due to its multifactorial mechanism as well as to rapid onset of the analgesic action, nimesulide represents an appealing therapeutic choice for the treatment of rheumatology patients.
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